Maternal prenatal omega-3 fatty acid supplementation attenuates hyperoxia-induced apoptosis in the developing rat brain.


Tuzun F., KUMRAL A., ÖZBAL S., Dilek M., TUĞYAN K., DUMAN N., ...Daha Fazla

International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience, cilt.30, sa.4, ss.315-23, 2012 (SCI-Expanded) identifier identifier identifier

Özet

Supraphysiologic amounts of oxygen negatively influences brain maturation and development. The aim of the present study was to evaluate whether maternal omega-3 long-chain polyunsaturated fatty acid (omega-3 FA) supplementation during pregnancy protects the developing brain against hyperoxic injury. Thirty-six rat pups from six different dams were divided into six groups according to the diet modifications and hyperoxia exposure. The groups were: a control group (standard diet + room air), a hyperoxia group (standard diet + 80% O-2 exposure), a hyperoxia + high-dose omega-3 FA-supplemented group, a hyperoxia + low-dose omega-3 FA-supplemented group, a room air + low-dose omega-3 FA-supplemented + group, and a room air + high dose omega-3 FA-supplemented group. The omega-3 FA's were supplemented as a mixture of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) from the second day of pregnancy until birth. Rat pups in the hyperoxic groups were exposed to 80% oxygen from birth until postnatal day 5 (P5). At P5, all animals were sacrificed. Neuronal cell death and apoptosis were evaluated by cell count, TUNEL, and active Caspase-3 immunohistochemistry. Histopathological examination showed that maternally omega-3 FA deficient diet and postnatal hyperoxia exposure were associated with significantly lower neuronal counts and significantly higher apoptotic cell death in the selected brain regions. Omega-3 FA treatment significantly diminished apoptosis, in the selected brain regions, in a dose dependent manner. Our results suggest that the maternal omega-3 FA supply may protect the developing brain against hyperoxic injury. (C) 2012 ISDN. Published by Elsevier Ltd. All rights reserved.